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Yves Pommier
Researcher at National Institutes of Health
Publications - 847
Citations - 65543
Yves Pommier is an academic researcher from National Institutes of Health. The author has contributed to research in topics: Topoisomerase & DNA. The author has an hindex of 123, co-authored 789 publications receiving 58898 citations. Previous affiliations of Yves Pommier include Purdue University & Kyushu University.
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Altered DNA topoisomerase II activity in Chinese hamster cells resistant to topoisomerase II inhibitors
TL;DR: A line of Chinese hamster cells characterized the resistance of which to the cytotoxic effect of intercalators and etoposide is associated with a reduced formation of protein-associated DNA strand breaks, and had an unusually high level of DNA linking activity in the absence of 4'-(9-acridinylamino)methanesulfon-m-anisidide.
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Topoisomerase I inhibitors: selectivity and cellular resistance.
TL;DR: Topoisomerase I (top1) inhibitors (camptothecins and other structurally diverse compounds) are effective and promising anticancer agents and determinants of selectivity toward cancer cells and resistance are multifactorial.
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Differential induction of apoptosis in undifferentiated and differentiated HL-60 cells by DNA topoisomerase I and II inhibitors
TL;DR: P phenotypic changes associated with TPA-induced differentiation include inactivation of a cytoplasmic activity that can induce DNA fragmentation associated with apoptosis, which is similar to drug-induced DNA fragmentation.
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Local sequence requirements for DNA cleavage by mammalian topoisomerase II in the presence of doxorubicin
TL;DR: Among 97 doxorubicin-stabilized sites that were localized at the DNA sequence level, none coincided with any of the 90 topoisomerase II cleavage sites detected in the same regions in the absence of drug, explaining the mutual exclusivity of the two classes of sites.
Journal Article
Correlations between intercalator-induced DNA strand breaks and sister chromatid exchanges, mutations, and cytotoxicity in Chinese hamster cells.
TL;DR: Data show that the DSB induced by 4'-(9-acridinylamino)methanesulfon-m-anisidide and 5-iminodaunorubicin at DNA topoisomerase II binding sites correlated closely with SCE, mutations, and cell killing and could therefore be responsible for their production.